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SF2- Exam 2 > Clinical Applications: Cranial Nerves > Flashcards

Clinical Applications: Cranial Nerves Flashcards

1
Q

What is the pathway of the olfactory nerve?

A
  1. The primary olfactory nerve cell bodies send central processes to synapse on secondary olfactory cells in the olfactory bulb.
  2. Seconday sensory axons then form the olfactory tract.

NOTE: The peripheral processes of the primary olfactory neurons are in the olfactory epithelium act as sensory receptors.

* Signals do not pass through thalamus

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2
Q

Where along the olfactory pathway can pathology occur?

A
  • The receptor
    • ​Temporary loss of smell results, most commonly from swelling and congestion
    • In rare cases, tumors of the epithelium can arise
  • The primary olfactory axon
    • ​ May result in permanent unilateral or bilateral anosmia and is frequently seen with fractures through the cribiform plate
  • The central pathway
    • ​Includes olfactory bulb, olfactory tract, and central projections
    • May be compressed from tumors, aneuryms of the anterior cerebral artery, and infiltrating tumors on frontal lobe
    • May result in unilateral or bilateral loss of smell
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3
Q

What is the pathway of the optic nerve?

A

CN II extends from the optic disc to the optic chiasm and continues as the optic tract to the lateral geniculate nucleus, pretectal nuclei, and superior colliculus.

*Optic nerve axons leave the eye, and blood verssels enter the eyer at the optic disc.

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4
Q

The retina can be divided into what two divisions?

A

An imaginary vertical line through the foveola divides the retina into the nasal hemiretina and the temporal hemiretina.

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5
Q

How is it possible for the optic nerve to be affected by MS?

A

The axons in the optic nerve, chiasm, and tract, like other central nervous system axons, are myelinated by oligodendrocytes. MS is a disease of oligodendrocytes.

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6
Q

What lesions of the visual pathway result in visual loss?

A
  • Anterior to the chiasm
    • ​Damge to the retina or optic nerve results in visual loss in the affected eye only (monocular visual loss)
  • At the chiasm
    • ​Damage to the optic chiasm usually results in loss of vision from both eyes
    • Damage to the midline of the chiasm results in loss of peripheral fields in both eyes (bitemporal hemianopia)
  • Posterior to the chiasm
    • ​Damage tot he optic tracts, lateral geniculate body, optic radiations, or visual cortices result in visual loss from both eyes within the contralateral visual field (homonymous hemianopia)
  • Lesions of Meyer’s loop
    • ​Results in homonymous quadrantanopia (loss of the contralateral upper visual field in both eyes
  • Partial loss of axons along the visual pathway
    • ​Scotomas
      • Blind spots
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7
Q

What is macula sparing?

A

The sparing of the central vision within the hemianopic hemifield

*Macular sparing signifies sparing of the posterior pole of the occipital lobe

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8
Q

What four procedures are used to exam the optic nerve?

A
  • Measurement of visual acuity (test macular function)
  • Testing of visual fields
  • Testing of the pupillary light reflex
  • Fundoscopy
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9
Q

Lesions of the parietal Radiations/upper lip of calcarine fissure can result in…

A

Contralateral homonymous inferior quadrantanopsia

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10
Q

Lesions of the temporal Radiations/lower lip of calcarine fissure can result in…

A

Contralateral homonymous superior quadrantanopsia

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11
Q

What can cause lesions of the optic nerve or components of the optic nerve?

A
  • Optic Neuritis- inflammation that damages the optic nerve
  • Multiple Sclerosis- disease of oligodendrocytes
  • Neuromyelitis Optica- inflammation and demyelination of the optic nerve (optic neuritis) and the spinal cord (myelitis)
  • Amaurosis Fugax – a painless temporary loss of vision in one or both eyes (occlusion of ophthalmic artery)
  • Papilledema- Increased Intracranial pressure
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12
Q

What disease is presented here?

A

Nothing. This is a normal fundoscopy

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13
Q

What disease is presented here?

A

Papilledema

*The lesion is in the optic disk​

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14
Q

What disease is presented here?

A

Atrophy

Causes of ONA include heredity, trauma (including stroke), a tumor, decrease in oxygen or blood supply, infections, or disorders.

Optic neuritis takes 4-6 weeks for nerves to atrophy.

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15
Q

What disease is presented here?

A

Central Retinal Artery Occlusion

Central retinal artery occlusion occurs when the central retinal artery becomes blocked, usually due to an embolus. It causes sudden, painless, unilateral, and usually severe vision loss.

*You don’t really see the disc here

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16
Q

What is the pathway of the oculomotor nerve?

A
  1. Axons of the oculomotor nucleus and the Edinger- Westphal nuclei course ventrally in teh midbrain to form the oculomotor nerve
  2. Ocumotor nerve emerges from the interpeduncular fossa on the ventral aspect of the midbrain
  3. After passing between the posterior cerebral and the superior cerebellar arteries, the nerve course anteriorly
  4. It pierces the dura and enters the cavernous sinus an then continues toward the superior orbital fissure
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17
Q

Which muscles are supplied by the oculomotor nerve?

A
  • Medial rectus muscle: Adduction
  • Superior rectus muscle: Elevation
  • Inferior rectus muscle: depression
  • Inferior oblique muscle: Excyclotorsion
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18
Q

How does the posterior communicating artery aneurysm cause a lesion of the oculomotor nerve?

A

CN III passes close to posterior communicating artery. An aneurysm of the posterior communicating artery can compress CN III, resulting in a lower motor neuron lesion

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19
Q

A lesion of CN III can result in a fixed, dilated pupil. Why?

A

There is damaged to the Edinger- Westphal nuclei which receives bilateral innervation from the optic nerve.

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20
Q

Where along the course of CN II can damage occur?

A
  • Nucleus of CN III (rare)
    • ​Due to trauma, ischemia, or demyelination within the midbrain
  • Peripheral axons
    • Damage to axons in the subarachnoid space
      • Diabetes
    • Due to anerysms (usually of the posterior communicating artery and sometimes int he basilar artery)
    • Due to uncus (of the temoral lobe) herniation
      • ​Due to raised intracranial pressure
    • Compression of axons in the cavernous sinus
      • Tumors
      • Inflammation
    • Damage could occur at the superior orbital fissure
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21
Q

Oculomotor divides into __________ and __________divisions

A

superior; inferior

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22
Q

What is the pathway of cranial nerve IV?

A
  1. Axons arising from the trochler nucleus course dorsally around the periaqueductal grey matter and cerebral aqueduct, and cross the midline.
  2. The crossed axons emerge from the dorsal aspect of the midbrain just caudal to the inferior colliculus to form cranial nerve IV.
  3. The nerve curves ventrally around the cerebral peduncle to pass between the posterior cerebral and superior cerebellar arteries.
  4. Cranial nerve IV runs anteriorly to pierce the dura at the angle between the free and attached borders of the tentorium cerebelli
  5. It enters the cavernous sinus, within the cavernous sinus, the trochlear nerve is situated between cranial nerves III and V1 and lateral to the internal carotid artery.
  6. It leaves the superior orbital fissure and course close to the orbit toward the superior oblique muscle
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23
Q

Which muscle is innervated by the trochlear nerve?

A

Superior oblique muscle

24
Q

Why does lesion of the trochlear nerve result in diplopia?

A

Because the superior oblique muscle is not working, it’s antagonist muscle, the inferior oblique muscle extors a slightly extorts and slightly elevates the problem eye.

25
Q

Which cranial nerve is the only cross cranial nerve?

A

The trochlear nerve

*It is also the only nerve to exit dorsum to the brainstem

26
Q

What are results of a lesioned trochlear nerve?

A
  • Contralateral Superior Oblique Muscle Paralysis – Eye does not depress when adducted.
  • Diplopia in the vertical plane when looking down and in
  • Compensation by head tilt
27
Q

What is trigeminal neuralgia?

A

It is a condition in which excrutiating paroxysms of pain occur in one or more divisions of the trigeminal nerve.

*The mandibular or maxillary divisions are most often involved.

  • Thought be due to local irritation of the sensory fibers in the trigeminal nerve.
28
Q

Where along the trigeminal sensory and motor pathways can pathologies occur?

A
  • Along the course of the peripheral nerves
    • ​Herpes Zoster virus
      • Affects the opthalmic division
  • Within the Middle Cranial fossa
    • ​Compression by a tumor
  • Within the central nervous system
    • ​Tumors, demyelinating disease, and vascular problems
    • Within the medulla, loss of pain and temperature sensation on ipsilateral side of the face can result
    • Within the pons, ipsilateral discriminative touch is primarily affected, affecting ipsilateral muscles of mastication (giving rise to a lower motor neuron lesion)
29
Q

Lesion of CN V leads to ipsilateral jaw deviation why?

A

Because of weakness of muscles of mastication like temporalis, masseters, and pterygoid muscles. The pterygoid muscles work unopposed.

30
Q

Trigeminal motor nucleus is located in _________

A

mid pons

31
Q

What are symptoms of a lesion of CN V?

A
  • Sensory deficit face
  • Absent corneal reflex (V1) – location: lateral medulla to upper cervical region
  • Motor deficit – weakness muscles of mastication (temporalis, masseters, pterygoids)
    • Leading to ipsilateral jaw deviation

NOTE: If you had an issue with CN 7 and were unable to blink as a result, that eye won’t blink but the opposite eye will still be able to blink. That wouldn’t be considered an absent corneal reflex since the inability to blink isn’t the result of an affected CN 5

32
Q

What is the course of CN VI?

A

Abducens nucleus (caudal pons) → inferior pontine sulcus → cavernous sinus (middle wall) → superior orbital fissure (sphenoid bone)

33
Q

What muscle is innervated by the abducens nerve?

A

Lateral rectus

34
Q

When CN VI most often affected?

A

The 6th cranial nerve is most commonly affected when there’s increased cranial pressure, without there being a direct lesion of the 6th cranial nerve

35
Q

What the results of a lesion in CN VI?

A
  • Paralysis of Lateral rectus
  • Diplopia in direction of action of paralyzed muscle
36
Q

Where along the course of CN VI could damage occur?

A
  • Within the brainstem
    • ​Infarction, tumorm demyelination
  • Betwen the brainstem and cavernous sinus
    • ​Nerve can become ischemic (diabetes)
    • Meningitis
  • Within the cavernous sinus
    • ​Carotid aneurysm, inflammation
  • Within the superior orbital fissure
  • ​Within the orbit
37
Q

What muscles are supplied by the facial nerve?

A

Muscles of Facial Expression & Orbicularis Oculi (eye closure)

38
Q

Lower motor lesions of CN VII result in…

A
  • Inability to close eye, wrinkle forehead, frown
  • Droop of angle of mouth, drooling of saliva, flattened naso-labial fold, inability to puff out cheek
  • Taste anterior 2/3rds of tongue – chorda tympani branch to V-3 division
39
Q

What is facial nerve palsy?

A

a neurological condition in which function of the facial nerve (cranial nerve VII) is partially or completely lost.

40
Q

There are two clinical manifestations of a CN VII lesion. What are they?

A

The facial nerve has an upper motor neuron type of weakness that it can experience in addition to a lower motor neuron type of weakness. This is based on the corticobulbar supply

  • The neurons of the facial nerve that supply the upper half of the face get bilateral (from both ipsi and contra-lateral sides) corticobulbar supply
  • The neurons of the facial nerve that supply the lower half of the face get contralateral corticobulcar tract supply only
    • Lesion to the contralateral corticobulbar tract/upper motor neuron of the CN will affect all the neurons of cranial nerve 7 to the lower part of the face because they are only innervated by the contralateral corticobulbar tract. The upper half of the face is still able to function because of the ipsilateral supply
    • A lesion to the contralateral side may result in drooping of the mouth/drooling, but you’ll still be able to blink.
    • A lesion at the nucleus or the nerve will lead to loss of muscle function in the half of the face that is supplied by that nerve. This would be known as a lower motor neuron lesion with ipsilateral effects
      • Patient will be unable to close eyes, wrinkle forehead, and frown on that side
41
Q

A lesion to the contralateral corticobulbar supply is also a lesion in the __________.

A

Upper motor neuron

42
Q

A lesion to the ipsilateral corticobular supply is also considered a lesion of the __________

A

Lower motor neuron

43
Q

What are results of a lesion to the upper motor neuron?

A
  • Sparing of upper part of face – bilateral cortico-bulbar supply
  • Weakness of only lower half of face on contralateral side – only unilateral contralateral corticobulbar supply
44
Q

A lesioned lower MN is also known as ____________.

A

Bell’s palsy

*Often viral in origin

45
Q

What can be some possible causes of a cranial nerve 7 lesion?

A
  • Bell’s Palsy
  • Guillain Barre syndrome- demyelinating disease
  • Lyme disease
  • Basal Meningitis (chronic)
  • Pontine lesions
46
Q

What are the results of a CN VIII lesion?

A

Auditory Nerve Lesions:

  • Hearing loss ipsilaterally
  • Tinnitus or ringing noises

Vestibular Nerve Lesions:

  • Vertigo
  • Nystagmus
  • The rapid involuntary movement of the eyes. There is a fast and slow component to this. The fast component is the correctional component. The direction of the nystagmus is always in the direction of the fast component.
47
Q

The 8th CN has an auditory component and a vestibular part (balance). Vestibular comes from the ____________ and the auditory comes from the __________.

A

semicircular canals; cochlea.

48
Q

What are possible causes of a lesion CN VIII?

A
  • Schwannoma (neurofibromatosis type II)
  • Acute labyrinthitis
    • Acute dizziness resulting from infections entering the labyrinth, maybe via a middle ear infection
  • Fractures of base of skull
    • Can cause hematoma behind the ear which can lesion the 8th CN
49
Q

Cranial nerve 9 and 10 can be tested in:

A
  • Swallowing
  • Phonation
  • Gag reflex
50
Q

What roles fo cranial nerves 9 and 10 play in gag reflex?

A
  • Sensations in the posterior pharynx are picked up by the 9th cranial nerve, it also picks up taste in the back of the throat.
  • Motor elevation of the soft palate (and pharyngeal and laryngeal muscles) is done by the 10th cranial nerve
51
Q

What symptoms result from a lesion of cranial nerve 9/10?

A
  • Nasal twang
  • Nasal regurgitation of liquids
  • Palate does not elevate
  • Absent gag reflex
52
Q

What disorders can cause lesion CNs 9 and 10?

A
  • Brain stem strokes – lateral medulla
  • Tumors
  • Basal meningitis
53
Q

What are possible causes on damage to CN XI?

A

Neck Tumor

54
Q

What symptoms result from leasion of the 12th cranial nerve?

A
  • Weakness ipsilateral half of tongue
  • Deviation to weak side on protrusion
  • Inability to push tongue over to opposite side
  • Atrophy, fasciculations of ipsilateral half
55
Q

What disorders can cause lesions of CN XII?

A
  • Amyotrophic lateral sclerosis ( motor neuron disease – bilateral – worm like tongue)
  • Tumors
  • Medial medullary lesions - stroke

SF2- Exam 2 (16 decks)

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